Abstract
Purpose :
Acute angle closure attacks are frequently accompanied by corneal edema. However, little is known about the status of corneal endothelial cells at early stages of angle closure in eyes naïve to prior surgery, iridotomy, or severe IOP elevation. Here, we compare endothelial cell density (ECD) in unoperated eyes with open angles and eyes at various stages of angle closure disease.
Methods :
This cross sectional study evaluated both eyes of sibling pairs recruited from one of 4 Aravind Eye Hospitals in Tamil Nadu, India, between September 2012 and May 2014. Masked examiners completed gonioscopic evaluation and eyes were classified as 1) open angle (OA), 2) primary angle closure suspect (PACS), or 3) primary angle closure/primary angle closure glaucoma (PAC/PACG). Specular microscopy was performed in both eyes and group differences in endothelial cell density were analyzed using a nested multilevel model with mixed effects to account for clustering at familial and individual levels.
Results :
Analyses included 814 eyes of 407 patients, including 127 eyes (15.6%) with PAC/PACG, 466 (57.3%) with PACS, and 221 (27.1%) with OA. Participants were predominantly female (69.8%) and mean age was 49.2 (SD: 8.6) years. Lower ECD was observed with increasing age (β =-6.3 cells/mm2 [95% CI: -9.3 to -3.3] per year, p<0.001), greater irido-trabecular contact (β =-15.6 cells/mm2 [95% CI: -28.3 to -2.9] per quadrant of contact, p=0.016), and shallow (<2.5mm) anterior chamber (AC) depth (β =-40 cells/mm2 [95%CI: 78.9 to 1.1] vs. deeper [>2.5 mm] AC depth, p=0.044). In age-adjusted analyses, PACS eyes had a lower ECD than OA eyes (β=-54.7 cells/mm2 [95% CI=-47.8 to -85.3], p=0.018) though PAC/PACG eyes were not significantly different than OA eyes (β=-18.6 cells/mm2 [95% CI=-85.9 to 2.5], p=0.058).
Conclusions :
Lower ECD may be present in eyes with angle closure, particularly those with a shallower AC and/or greater iridotrabecular contact, even prior to initiation of treatment. Additional longitudinal studies are needed to further establish whether these factors are associated with higher rates of endothelial cell loss.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.